Cardio part 1 Flashcards

1
Q

Pathophys of infective endocarditis

A

Bacteremia that delivers the organisms to the surface of the valve
Adherence of the organisms
Eventual invasion of the vavular leaflets

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2
Q

Etiology of endocarditis

A
Native valve:
Rheumatic valvular disease- primarily involving the mitral valve
Congenital heart disease
Mitral valve prolapse
Degenerative heart disease
Prosthetic valve endocarditis:
Local abscess and fistula formation, valvular dehiscence
IVDA
New therapeutic modalities
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3
Q

S/sx of infective endocarditis

A
Fever
Chills
Anorexia
Wt loss
Malaise
HA
Myalgias
Night sweats
SOB
Cough
Joint pains
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4
Q

What is the difference between acute and subacute endocarditis?

A

Subacute is characterized by a hx of an indolent process
Subacute process is caused by S. viridans
Interval between onset and dx averages about 6 wks
Acute is much more aggressive

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5
Q

PE of infective endocarditis

A
Fever
Heart murmur
Petechiae
Subungual hemorrhages
Osler nodes
Janeway nodes
Roth spots
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6
Q

Workup of infective endocarditis

A
CBC
CMP
Glucose
Coag panel
UA
Three sets of blood cultures
Echo- transthoracic
U/s
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7
Q

Tx of infective endocarditis

A

Treat any congestive heart failure
Native valve- pen G and gentamicin
IVDU- vanc and gentamicin
Prosthetic valve- Vanc and gentamicin and rifampin
Consider linezolid sub for vanc with unstable renal function

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8
Q

Indications for surgery in infective endocarditis

A

CHF refractory to standard medical therapy
Fungal infective endocarditis (except H. capsulatum)
Persistent sepsis after 72 hrs of appropriate antibiotic tx
Recurrent septic emboli
Rupture of an aneurysm of the sinus of Valsalva
Conduction disturbances caused by a septal abscess
Kissing infection of the anterior mitral leaflet in pts with IE of the aortic valve

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9
Q

Pathophysiology of angina pectoris

A

Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand
Angina pectoris is the MC clinical manifestation of myocardial ischemia
Caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium

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10
Q

Precipitating factors of angina pectoris

A
Severe anemia
Fever
Tachyarrhythmias
Catecholamines
Emotional stress
Hyperthyroidism
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11
Q

S/sx of angina pectoris

A
Retrosternal chest discomfort:
-Pressure
-Heaviness
-Squeezing
-Burning
-Choking sensation
Locations:
-Epigastrium
-Back 
-Neck
-Jaw
-Shoulders
Radiation:
-Arms
-Shoulders
-Neck
Precipitated by exertion, eating, exposure to cold, or emotional stress
Stable: Lasts 1-5 mins and relieved by rest of nitroglycerin
Intensity does not change with respiration, cough, or change in position
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12
Q

PE of angina pectoris

A

Positive Levine sign

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13
Q

Workup of angina pectoris

A

CXR
Exercise stress test
Stress echo
Nuclear imaging for those with baseline EKG abnormalities
EKG
Procedures for those with inconclusive noninvasive study results or unstable angina despite maximal medical tx

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14
Q

Tx of angina pectoris

A
Treat RFs
-Statins
Daily aspirin
Nitro
Beta blockers
Lifestyle modifications
Consider revascularization with left main artery stenosis >50%, 2- or 3-vessel dz and LV dysfunction, poor prognostic signs during noninvasive studies, or severe sx despite maximum medical therapy
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15
Q

Pathophys of atrial fibrillation

A

Electrical remodeling
Contractile remodeling
Structural remodeling

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16
Q

RFs of AFib

A
Hemodynamic stress
Atrial ischemia
Inflammation
Noncardiovascular respiratory causes
EtOH and drug use
Endocrine d/os
Neurologic d/os
Genetic factors
Advancing age
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17
Q

S/sx of AFib

A
Wide variety
Palpitations
Dyspnea
Fatigue
Dizziness
Angina
Decompensated heart failure
Poor exercise tolerance
Presyncope or syncope
Generalized weakness
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18
Q

PE of AFib

A

Irregularly irregular pulse
Tachycardia
May have exophthalmos, thyromegaly, elevated JVP, or cyanosis
May have heart failure, wheezes, or diminished breath sounds
May have displaced PMI or S3
Prominent P2 with pulmonary HTN
May have ascites, hepatomegaly, or hepatic capsular tenderness
Cyanosis, clubbing, or edema of lower extremities

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19
Q

Workup for AFib

A
EKG
CBC
Serum electrolytes and BUN/creatinine
CK and/or troponin
BNP
D-dimer
Thyroid function studies
Digoxin level
Toxicology testing or ethanol level
Echo
CTA if D-dimer pos
CT or MRI if ablation is planned
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20
Q

RFs of stroke in pts with AFib

A
Advancing age
Female
HTN
DM
Heart failure
Hx of stroke/TIA/thromboembolism
CAD
PAD
Valvular heart disease
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21
Q

Management of new-onset AFib

A

BBs and CCBs are 1st line for rate control
Amiodarone for those intolerant or unresponsive to other agents
Anticoagulation
Cardioversion may be necessary

22
Q

When should cardioversion be done on an AFib pt?

A
Hemodynamically unstable
Severe dyspnea or CP
Preexcited AFib
Rate-control is not working
Echo does not reveal any valvular or functional abnormality of the heart
23
Q

Pathophys of atrial flutter

A

Single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus, with an area of slow conduction between tricuspid valve annulus and the coronary sinus ostium

24
Q

Etiology of atrial flutter

A
Coronary artery disease
Hypertensive heart disease
Rheumatic heart disease
Congenital heart disease
Pericarditis
Cardiomyopathy
Hypoxia
COPD
PE
Hyperthryoidism
Pheochromocytoma
DM
Electrolyte imbalance
EtOH consumption
Obesity
Digitalis toxicity
Myotonic dystrophy in childhood
25
Typical sx of atrial flutter
Palpitations Fatigue or poor exercise tolerance Mild dyspnea Presyncope
26
Less common sx of atrial flutter
Angina Profound dyspnea Syncope
27
Workup for atrial flutter
``` EKG Vagal maneuvers if flutter waves are not seen Adenosine Exercise testing TTE ```
28
Tx of atrial flutter
CCBs or BBs for rate control May need cardioversion Anticoagulation Consider radiofrequency ablation
29
Etiology of SVT
``` Triggered by a reentry mechanism Premature atrial or ventricular ectopic beats Other triggers: -Hyperthyroidism -Stimulants -Alcohol ```
30
Hs and Ts of arrhythmias
``` Toxins Thromboses Temperature Tension pneumo Tamponade Trauma Hypoxia Hypovolemia Hypokalemia/hyperkalemia Hydrogen ```
31
Common sx of SVT
``` Palpitations Dizziness SOB Syncope CP Fatigue Diaphoresis Nausea ```
32
Workup of SVT
``` Cardiac enzymes Electrolyte levels CBC Thyroid studies Digoxin level Electrophysiologic studies EKG CXR TTE ```
33
Tx of SVT
Hypotensive or unstable: immediate cardioversion | Stable: try vagal maneuvers, then if unsuccessful, adenosine
34
Pathophys of VTach
Caused by electrical reentry or abnormal automaticity
35
Caused by electrical reentry or abnormal automaticity
``` Ischemic heart dz Structural heart dz with disruption of nl conduction patterns Congenital structural cardiac d/os Acquired channelopathies Inherited channelopathies Electrolyte imbalances Sympathomimetic agents Digitalis toxicity Systemic diseases causing infiltrative cardiomyopathy or scar ```
36
S/sx of VTach
``` Palpitation Lightheadedness Syncope CP Can also be asymptomatic ```
37
PE of VTach
``` Hypotension Tachypnea Diminished LOC Pallor Diaphoresis High JVP Mental status changes: Anxiety Agitation Lethargy Coma ```
38
Workup of VTach: labs
Electrolytes Serum levels of therapeutic drugs Toxicology Serum cardiac markers
39
Workup of VTach: imaging, other
Echo EKG Holter monitoring with recurrent syncope or palpitations
40
Tx of VTach: stabilization
VT associated with loss of consciousness or hypotension needs immediate cardioversion with 100-200J biphasic Address reversible RFs Lidocaine if pts have ongoing myocardial ischemia Pulseless VT- high-dose unsynchronized energy
41
Tx of VTach: postabilization management
Referral to a cardiologist Admission to a monitored bed Further studies, such as electrophysiologic study Consideration for radiofrequency ablation Consideration for ICD placement
42
Tx of VTach: long-term tx
Depends on cause: Amiodarone in combo with BBs for pts with left ventricular dysunction d/t previous MI Heart failure: BB, ACE, aldosterone antagonists Stains for coronary heart disease
43
Pathophys of VFib
Most often associated with CAD Can result from AMI or ischemia or from myocardial scarring from an old infarct VTach can aslo degenerated into VFib Reentrant patterns break up into multiple smaller wavelets and the level of disorganization increases, with reentrant circuits producing high-frequency activation of cardiac muscle fibers
44
Etiology of VFib
``` Acute and chronic ischemic heart disease Valvular disease Congenital structural heart disease Paroxysmal VFib or short-coupled torsades Idiopathic VFib and VTach PE Aortic dissection Electronic control devices Nonstructural abnormalities Catecholaminergic polymorphic VTach WPW syndrome Brugada syndrome ```
45
Presentation of VFib
Pts at risk may have prodromes of CP, fatigue, palpitations, and other nonspecific complaints, but many are asymptomatic
46
What is the single greatest RF for sudden death from VF?
Hx of left ventricular dysfunction
47
Considerations when thinking about VFib?
``` CAD Previous cardiac arrest Syncope or near-syncope Prior MI, esp within 6 mos LVEF <30-35% H/o frequent ventricular ectopy Drop in SBP or ventricular ectopy upon stress testing, particularly when associated with acute myocardial ischemia Dilated cardiomyopathy from any cause HCM Use of inotropic meds Valvular heart disease Myocarditis ```
48
Triggers of VFib
Antiarrhythmic drug administration Hypoxia Ischemia Atrial fibrillation with very rapid ventricular rates in the presence of preexcitation Electric shock administered during cardioversion Electric shock caused by accidental contact with improperly ground equipment Competitive ventricular pacing to terminate VTach
49
Workup for VFib
``` Confirm only with EKG Echo Nuclear imaging for assessment of pts at risk Labs: 'lytes, including calcium and magnesium Cardiac enzymes CBC ABG Quantitative drug levels Tox screens and levels TSH BNP ```
50
Tx of VFib
Defibrillation Postresuscitation: Admit to ICU with close monitoring Assess for complications and establish the need for emergent interventions Mild therapeutic hypothermia BBs Thorough diagnostic testing to establish underlying etiology
51
When is radiofrequency ablation indicated for the prevention of VFib?
AV bypass tracts Bundle branch block ventricular tachycardia Right ventricular outflow tract tachycardia Idiopathic left ventricular tachycardia Idiopathic VFib Rare forms of automatic focal VTach Scar-related VTach due to ischemic or nonischemic myopathy